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Thoracic myelocystocele are extremely rare, non-terminal, closed neural tube defects. Intraoperative neuromonitoring (IONM) is a mainstay of pediatric spinal surgery. However, in neonates and infants, incomplete myelination of the corticospinal tract presents unique challenges to successful use of IONM in this vulnerable patient population. Surgery can often be delayed until patients are older, but there are circumstances in which early intervention is necessary. We report a case of T6 myelocystocele resection and wound closure in an infant on day of life 15 with the use of IONM. To our knowledge, this is the youngest reported patient to undergo successful IONM in the spinal cord. Given that the majority of thoracic myelocystoceles present without any neurological deficits, early intervention for this rare closed spinal dysraphism is sometimes necessary. This case study reports the possibility of IONM use in neonatal patients and also highlights the techniques that make its use more possible. [ABSTRACT FROM AUTHOR]

Glucocorticoids exert an opposing rapid regulation of glutamate and GABA synaptic inputs to hypothalamic magnocellular neurons via the activation of postsynaptic membrane-associated receptors and the release of retrograde messengers. Glucocorticoids suppress synaptic glutamate release via the retrograde release of endocannabinoids and facilitate synaptic GABA release via an unknown retrograde messenger. Here, we show that the glucocorticoid facilitation of GABA inputs is due to the retrograde release of neuronal nitric oxide and that glucocorticoid-induced endocannabinoid synthesis and nitric oxide synthesis are mediated by divergent G-protein signaling mechanisms. While the glucocorticoid-induced, endocannabinoid-mediated suppression of glutamate release is dependent on activation of the Gαs G-protein subunit and cAMP-cAMP-dependent protein kinase activation, the nitric oxide facilitation of GABA release is mediated by Gβγ signaling that leads to activation of neuronal nitric oxide synthase. Our findings indicate, therefore, that glucocorticoids exert opposing rapid actions on glutamate and GABA release by activating divergent G-protein signaling pathways that trigger the synthesis of, and glutamate and GABA synapse-specific retrograde actions of, endocannabinoids and nitric oxide, respectively. The simultaneous rapid stimulation of nitric oxide and endocannabinoid synthesis by glucocorticoids has important implications for the impact of stress on the brain as well as on neural-immune interactions in the hypothalamus. [ABSTRACT FROM AUTHOR]